It has been assumed, since the pioneering work of Krogh (340,341), that the capillary bed in skeletal muscle mainly serves to supply oxygen, and this aspect has been emphasized in most studies of muscle as well as heart microvasculature. This is not surprising, as it has also been known for a long time (489) that red muscles, subsequently characterized by highly aerobic metabolism, have a much more dense capillary network than white muscles with glycolytic metabolism and that capillary density (CD) in the heart is almost an order of magnitude higher than it is in glycolytic muscles. However, capillaries are also needed for removal of different metabolites, one of the most important in skeletal muscle being lactate, and heat produced during muscle contraction. Nevertheless, it is far from clear to what extent oxygen demand or accumulation of waste products regulates capillary growth.

There are numerous accounts of capillary growth in developing heart or skeletal muscles and some concerning growth under pathological conditions such as regeneration or hypertrophy, but relatively little is known about growth in adult tissue. This is to be expected, since endothelial cells, not only in capillaries but also in large arteries, represent a very stable population of cells with very low mitotic activity (633). Capillary growth in adult skeletal or cardiac muscle has been described during endurance training; in skeletal muscle during longterm electrical stimulation; in chronically bradycardially paced hearts (for review see Ref. 283); during longterm administration of vasodilating drugs as well as during hypoxia, although this has recently been disputed (320, 464); and in skeletal (85) and cardiac (97) muscle of animals treated with thyroid hormones. Despite this mass of data it is still unclear what induces development and adaptation of the capillary bed, which differs within one muscle with respect to different types